Photodamaged or sun damaged skin occurs with exposure to sunlight (UVA or UVB). Twenty five percent of our lifetime exposure occurs before the end of our teenage years. Photodamage is considered to be the structural and functional deterioration of chronically sun-exposed skin. Keratinocytes, melanocytes, fibroblasts and endothelial cells are altered by UV radiation resulting in changes in skin texture, altered skin tightness and thickness, sallowness, dyschromia, wrinkles, telangiectasias, erythema, sebaceous gland hypertrophy and epithelial atypia or dysplasia (Baumann L. J Pathol. 2007 January; 211(2):241-51. Skin ageing and its treatment; Han A. Photoaging. Dermatol Clin. 2014: 291-9).
For the most part these changes occur most frequently on areas of chronic exposure including the face, ears, neck, backs of the hands, chest, arms and legs. Buttocks or upper inner arms are often preserved and pristine emphasizing the difference between chronological aging and photoaging.
As the manifestations of photodamage are numerous many options of treatment are proposed, such as: chemical peels, dermabrasion, injectable fillers, botulinum toxin and surgery, as well as topical treatments such as the use of retinoids and lately ablative and non-ablative resurfacing lasers carbon dioxide laser, ND-Yag, Q-switched, KTP and pulsed-dye lasers and intensed pulsed light (IPL)), radiofrequency and photodynamic therapy (PDT) as alternatives. (Shamban A T. Current and new treatments of photodamaged skin. Facial Plast Surg. 2009 December; 25(5):337-46.)
Nowadays photodynamic therapy (PDT), a recognized and approved treatment for nonmelanoma skin cancers and their precursors such as actinic keratosis, as well as for other organ and mucosal epithelial conditions, sees its indications enlarging to inflammatory or infectious conditions (e.g. psoriasis, acne, leishmaniosis). PDT involves the application of a photosensitizing (photochemotherapeutic) agent to the affected area of the body, followed after an incubation period to the exposure to a photoactivating light that will convert the photosensitizing agent into a cytotoxic form, followed by necrosis and apoptosis of the target tissue
A range of photosensitizing agents is known, including the psoralens, the porphyrins (e.g. Photofrin (Registered trademark)), the chlorins and the phthalocyanins. Amongst the most clinically useful photosensitizing agents known in the art, however, are 5-aminolevulinic acid and its derivatives, for example esters such as 5-ALA esters. These, through an intra cellular metabolism will be converted by the haem biosynthetic pathway predominantly to protoporhyrin IX (PpIX).
The mechanism of action of PDT relies on intracellular porphyrins (including PpIX) that are photoactive, fluorescing compounds and, upon light activation in the presence of oxygen, singlet oxygen is formed which causes damage to cellular compartments, in particular the mitochondria. Light activation of accumulated porphyrins leads to a photochemical reaction and thereby phototoxicity to the light-exposed target cells.
Although PDT is clinically useful in the treatment of a wide range of diseases, a major drawback of such treatment is the concomitant side-effects, particularly at the treatment site. These often include inflammation such as erythema, swelling, edema, burning, itching, exfoliation, hyperpigmentation and prolonged irritation and hypersensitivity after treatment. Such side-effects are particularly undesirable when the treatment site is the face, scalp or neck.
A need still therefore exists for alternative PDT methods especially using natural daylight with reduced or no undesirable side effects (e.g. inflammation, pain, etc.) as well as lower downtime but which have high therapeutic efficacy.